Patients with ischemic heart disease experience a wide range of pathological changes. Some of these include ventricular dilatation, dilatation of the mitral annulus, papillary muscle displacement and tethering, papillary infarcts, segmental and global ventricular dysfunction. The mitral valve function and competency rests on the fine geometric and functional integrity of its supporting structures.
When the left ventricle distorts due to dilatation or scarring from myocardial infarction, the papillary muscles are tethered, thus preventing adequate closure of the mitral valve. The left ventricle has two papillary muscles. Both originate from the left ventricular free wall. The anterior papillary muscle is attached to the anterior wall of the left ventricle, close to its lateral border. The posterior papillary muscle originates from the posterior wall, near the junction of the interventricular septum. The mitral valve closure is effected by the apposition of its leaflets. Papillary muscle tethering has been shown to be one of the important mechanisms resulting in mitral valve incompetency, and failure of leaflet apposition. Ischemic mitral regurgitation accounts for significant mortality and morbidity in patients with heart disease (it doubles the late mortality after heart attack and after bypass surgery if unrepaired).
FIG. 1 illustrates the fundamental problem of ventricular dilatation in a heart 2 and its relation to atrioventricular valve regurgitation. (Please note that the view presented is inverted from the normal anatomic presentation, as the heart depicted in this and other figures herein are presented as observed in an ultrasound image, with the apex 4 displayed on top because it is closest to the ultrasound transducer.) A damaged muscular wall 6 of a left ventricle 8, the heart's primary pumping chamber, becomes distorted and bulges outward from the center of the ventricular cavity 9. This displaces the papillary muscle 10, to which mitral valve leaflets 12 are anchored by a network of tendinous chords 14, in turn pulling on the leaflet tips and preventing proper meeting (i.e., coaptation) of the leaflets. This results in improper closure and mitral regurgitation from the left atrium 16 back into the left ventricular cavity 9 across the mitral annulus 18. Such regurgitation can produce heart failure, rhythm disorders, sudden death, and a predisposition to lethal heart valve infections. Even in patients in which ventricular remodeling has not yet resulted in significant atrioventricular valve regurgitation, dilatation causes a greater ventricular cavity volume and a commensurate increase in pumping load on the heart.
Previous work that addressed ischemic mitral regurgitation includes:
(a) Czer et al. documented that revascularization (Coronary Artery Bypass Grafting) alone does not improve mitral regurgitation. In a study of 2000 patients who underwent coronary artery bypass surgery, uncorrected mitral regurgitation nearly doubled the risk of late death.
(b) Mitral valve annuloplasty addresses the mechanism of annular dilation as a cause of ischemic mitral regurgitation. Mitral ring annuloplasty involves sewing a prosthetic mitral ring around the mitral annulus to reduce annular size and force the leaflets of the mitral valve to close better. Clinical observations suggest, however, that it does not always reduce the degree of MR because it does not correct for improper heart geometry. In addition, annuloplasty techniques involve opening the heart, an invasive procedure with significant associated risk, and requires placing the patient on cardiopulmonary bypass (stopping the heart and opening it to insert the ring while using an artificial pump to bypass the heart and lungs). To assess the efficacy of a procedure, one must examine mitral valve function once the heart has been released fully from cardiopulmonary bypass. If the surgical annuloplasty procedure failed to accomplish its objective, then one must reinstitute cardiopulmonary bypass to readjust the ring position. Repetitive cycles of cardiopulmonary bypass increase the already significant morbidity and mortality of surgical mitral ring annuloplasty. Because of these associated risks, surgical mitral ring annuloplasty is often not offered to the sickest patients who might otherwise gain the greatest benefit from the procedure.
(c) Surgical techniques have been advocated for surgically grasping the valve leaflets and stitching them together with a suture or other fastener. There are several difficulties that limit the ability to practice those inventions successfully. In patients with sufficient MR to warrant such procedure, the leaflets are initially misaligned, limiting or precluding the ability of a single device to bring the leaflet tips into juxtaposition in order to suture or fasten them together. Also, in order to be effective, the proposed suction device for grabbing the leaflets must withdraw blood extremely rapidly; unless blood is reinfused immediately, hypotension can ensue. A means for stabilizing the leaflet surfaces must also be utilized, otherwise the suture or staple intended to fasten the leaflets may instead displace them. Also, when the leaflets are overstretched, suturing may not be successful as suturing may increase the tension on the leaflets.
(d) Other ventricular remodeling techniques and patents have been introduced for restraining ventricular size, such as pericardial clamps or harnesses, in some cases having balloons or stakes affixed to them. Such devices encircle the heart in global ventricular dilatation and do not address specific segmental pathology, (i.e., they do not provide selectivity of the target points nor adaptability.) Other devices include passive tensor mechanisms that are inserted through the heart and have as their goal the reduction of ventricle diameter at that point. Permanently implanting components traversing the chambers of the heart is, again, a quite invasive treatment. And these approaches lack precise targeting or sturdy fixation. Rather, such techniques and/or devices have targeted a circumferential change in ventricular geometry versus a specific regional change in displacement, tension, and force. Precise targeting and correction of the stress strain and displacement interactions are specifically important for the intricate geometry of atrioventricular valves.
Thus, what is needed are methods and devices for treating ventricular remodeling and atrioventricular regurgitation by locally addressing the geometric distortion of the supporting structures of the ventricle.
It would additionally be desirable if such a technique could be performed without requiring cardiopulmonary bypass, the need for which frequently influences surgeons not to repair valves, particularly in patients who are more seriously ill and could benefit most from this repair, but are at greatest risk from prolonged bypass.
Further, because damage to heart geometry is also progressive, initial success in reducing regurgitation and/or remodeling is often followed by its recurrence. It would therefore be desirable to employ an approach to addressing these conditions that is adjustable over time.